Interferon alpha-7 (IFNA7)

Interferon alpha-7 (IFNA7) is a cytokine belonging to the type I interferon family, which plays a central role in innate immune defense, particularly against viral infections[1][2][5]. IFNA7 is primarily produced by macrophages and stimulates the production of antiviral proteins, including protein kinase and oligoadenylate synthetase[2]. Expression of IFNA7 is distinct from other interferon-α subtypes, being preferentially induced by the transcription factor IRF7, which is thought to support a delayed yet sustained type I interferon response during viral infection[1]. IFNA7 can trigger natural killer cell cytotoxicity but generally requires higher concentrations than other interferon-alpha subtypes[1]. Genetic variation in the IFNA7 gene has been associated with clinical outcomes in diseases such as colorectal cancer, highlighting its prognostic potential[1]. IFNA7 is active in the extracellular space and exerts its effects by signaling through the type I interferon receptor, leading to downstream JAK-STAT activation and broad transcriptional responses in target cells[1][2]. Although widely studied as part of the interferon-alfa group—several of which are therapeutic agents for viral and certain malignant diseases—no currently approved drugs selectively target IFNA7. The safety profile is similar to other type I interferons, involving common cytokine therapy adverse effects such as flu-like symptoms and risk of immune-mediated adverse events[2]. In summary, IFNA7 is an immunomodulatory, protein-coding gene involved in antiviral defense, immune signaling, and clinical immune modulation, with significant translational implications for infection, cancer, and inflammation[1][2][5].

Other names

IFN-alpha-7Interferon alpha-7IFNA-JIFN-alphaJIFN-alpha-J1IFN-alphaJ1Interferon alpha-JInterferon alpha-J1LeIF JIFNA7_HUMANIFNA-J1

Activation of type I interferon receptor (IFNAR1/2); induction of antiviral proteins (e.g., protein kinase, oligoadenylate synthetase); stimulation of JAK-STAT signaling pathway leading to transcription of ISGs (interferon-stimulated genes).